The following paragraphs are provided by way of background to the present disclosure. They are not however an admission that anything discussed therein is prior art or part of the knowledge of persons skilled in the art.
It is estimated that traumatic brain injury (TBI) and stroke collectively cost the Canadian and American medical systems 110 billion dollars annually (Finkelstein, Corso, and Miller, 2006; Heidenreich et al., 2011; Public Health Agency of Canada, 2009). Both TBI and ischemic stroke are characterized by the death of neural tissues, which initiates a molecular signaling cascade that induces the formation of astroglial scar tissue that protects surrounding tissue from further damage. However, this scar tissue can also inhibit neuronal regrowth or regeneration, and thus functional recovery. Currently, ischemic stroke therapies are directed at emergency care, notably at dissolving or removing blood clots. While these immediate care stroke treatments substantially limit the acute neural damage to a stroke patient by targeting the direct causal agent, and while these known treatments, if initiated in a timely manner, save lives, they are not effective in regenerating injured or destroyed neuronal cells. Hence stroke symptoms, such as cognitive, motor, and memory impairments, are commonly experienced by surviving stroke patients, and are frequently permanent. It is therefore desirable to develop effective medical therapies that replace damaged or destroyed neurons, or reduce the inhibitory astroglial scar to promote recovery and alleviate these functional deficits. The efficacy of the heretofore known therapeutic methodologies to restore neurons and astroglial scar is limited. Therefore there exists a need in the art for methods to restore functional neurons following stroke or TBI.